Mentions:
Mice were treated by osmotic mini-pump for 4 weeks with neutralizing Anti-ASP or control non-immune IgG (NI-IgG). Plasma samples were taken 9 days after implantation of the osmotic pump and at the end of the study to track the amount of antibody delivered into circulation. Figure 2A shows that on day 9 rabbit NI-IgG and Anti-ASP antibodies were detected (~4% of starting material). However, by the end, the levels of both NI-IgG and Anti-ASP were greatly reduced (~0.1% of starting material). Since there was no difference in osmotic mini-pump rate for PBS, rabbit antibodies or rASP treatments (data not shown), reduced antibody levels may be attributed to enhanced antibody clearance. Anti-ASP blocking antibody treatment had no effect on mouse body weight (NI-IgG: 29.2 ± 0.4 g and Anti-ASP: 29.6 ± 0.3 g, NS, n = 6-7), average food intake (NI-IgG: 13.8 ± 0.5 kcal/day and Anti-ASP: 14.3 ± 0.5 kcal/day, NS, n = 6-7) or food efficiency (NI-IgG: 200.1 ± 21.2 kcal/g and Anti-ASP: 165.6 ± 25.8 kcal/g, NS, n = 6-7), consistent with our previous report during a 10 day study [17]. There was also no difference in adipose tissue depots, liver or spleen weight between the two groups (data not shown). IL-6 levels were slightly but significantly elevated in Anti-ASP mice (P < 0.05, Figure 2B). However, CRP levels, a marker of inflammation, were normal (Figure 2C). Anti-ASP did not have an effect on fasting glucose levels after nine days of treatment (NI-IgG: 6.22 ± 0.62 mmol/L and Anti-ASP: 6.58 ± 0.54 mmol/L, NS, n = 6-7). Furthermore, there was no difference in plasma adiponectin, insulin, C3, or lipid levels between the two groups at the end of the study (Table 1).

Mentions:
Mice were treated by osmotic mini-pump for 4 weeks with neutralizing Anti-ASP or control non-immune IgG (NI-IgG). Plasma samples were taken 9 days after implantation of the osmotic pump and at the end of the study to track the amount of antibody delivered into circulation. Figure 2A shows that on day 9 rabbit NI-IgG and Anti-ASP antibodies were detected (~4% of starting material). However, by the end, the levels of both NI-IgG and Anti-ASP were greatly reduced (~0.1% of starting material). Since there was no difference in osmotic mini-pump rate for PBS, rabbit antibodies or rASP treatments (data not shown), reduced antibody levels may be attributed to enhanced antibody clearance. Anti-ASP blocking antibody treatment had no effect on mouse body weight (NI-IgG: 29.2 ± 0.4 g and Anti-ASP: 29.6 ± 0.3 g, NS, n = 6-7), average food intake (NI-IgG: 13.8 ± 0.5 kcal/day and Anti-ASP: 14.3 ± 0.5 kcal/day, NS, n = 6-7) or food efficiency (NI-IgG: 200.1 ± 21.2 kcal/g and Anti-ASP: 165.6 ± 25.8 kcal/g, NS, n = 6-7), consistent with our previous report during a 10 day study [17]. There was also no difference in adipose tissue depots, liver or spleen weight between the two groups (data not shown). IL-6 levels were slightly but significantly elevated in Anti-ASP mice (P < 0.05, Figure 2B). However, CRP levels, a marker of inflammation, were normal (Figure 2C). Anti-ASP did not have an effect on fasting glucose levels after nine days of treatment (NI-IgG: 6.22 ± 0.62 mmol/L and Anti-ASP: 6.58 ± 0.54 mmol/L, NS, n = 6-7). Furthermore, there was no difference in plasma adiponectin, insulin, C3, or lipid levels between the two groups at the end of the study (Table 1).

Bottom Line:
Again, there was no change in circulating insulin, adiponectin, CRP or TG levels, however, plasma free fatty acids were reduced (-48%, P < 0.05).In vitro, Anti-ASP effectively neutralized ASP stimulated fatty acid uptake.Therefore, ASP is a potent anabolic hormone that may also be a mediator of energy expenditure.